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CVS > Autonomic pharmacology > Flashcards

Autonomic pharmacology Flashcards

1
Q

What do PNS pre and post galnglonic neurones rleease

A

ACh

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2
Q

What do SNS pre and post ganglionic synpases release

A

Pre: ACh
Post”: NAd

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3
Q

What do most autonomic drugs target

A

target junctional communication so from post ganglionic neurones and the heart or blood vessel

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4
Q

What is the effect of sympatehtic stimulation

A
  • Increases heart rate and contractility (beta 1 receptor )
  • vasoconstriction (alpha 1 and 2)
  • some vasodilation (beta 2)
  • regulations of renin release for volume control (beta 1)
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5
Q

Which receptor increases HR and contractility

A

Beta 1 adrenorepcetor

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5
Q

Which recpetor can cause vasoconstriction

A

alpha 1 and 2

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6
Q

which receptor can cause vasodilation

A

beta 2

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7
Q

Name a drug that is an alpha 1 agonist

A

midodrine

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7
Q

Name an alpha 2 agonist

A

clonidine

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7
Q

Name a beta 1 agonist

A

dobutamine

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8
Q

Name a beta 2 agonist

A

Salbutamol

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9
Q

Name a alpha 1 antagonust

A

doxazosin

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10
Q

Name an beta 1 anatgonist

A

metoprolol

beta blocker

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11
Q

What happens if you activate a beta adrenoreceptor 1

A
  • increased heart rate (positive chronotropic effect)
  • Increased contractility rate (positive inotropic effect)
  • Increased automaticity
    • tendency to induce a spontaneous rhythm
    • important when heart is not generating any rhythm during asytole
    • important for use of adrenaline in resuscitation
  • Fast relaxation and recovery (lusitropic effect)
    • important for cardiac filling
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12
Q

How does a beta 1 agonist work

so like the mechanism

A

Beta 1 mediated pathway → will activate Gs → adenyl cyclase → cAMP, and PKA

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13
Q

beta 1 agonist mechanism

What does PKA target

A
  • Increass ICa,L (Ca2+ channel) for greater Ca2+ entry
  • Increased IK for faster repolarization
  • Increased Na+/K+ ATPase activity

-Increased If (funny current) for positive chronotropic

  • Increased SR Ca2+ uptake (via phospholamban inhibition of SERCA)
    • important for lusitropic effect, once ca2+ is released it needs to be removed by SERCA.
    • BY increasing rate of reuptake, cardiomyocytes can remove calcium quicker which means faster relaxation
  • Increased Ca2+ sensitivity
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14
Q

Clinical use of agonists

What is the clinical use of adrenaline

A

anaphylaxis
- (you have massive vasodilation, so having alpha 1 agonist opposes alpha one dilation)
-asystole (no electrical rhythm) ventricular fibrillation (after you’ve done DE-fib and other severe arrhythmias (low cardiac output)

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15
Q

What is the mechanism that adrenaline works by

so what recpetor does it bind to, and what does it do

A

when injected locally → causes vasoconstriction (at alpha 1 adrenoreceptors)

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16
Q

what can adrenaline be mixed with

A

local anasethtics

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17
Q

What receptor does dobutamine act on

A

beta 1 adrenoreceptors

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18
Q

is Dobutamine an agonist

A

Yes

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19
Q

agonists clinical uses

How does dobutamine work

A

α1 adrenoreceptor coupled to Gq -> Activation of IP3 -> IP3-mediated Ca2+ release from SR -> causes contraction.

alternative pathways PKC, and Rho-kinase
If you are wondering why it’s a beta 1 and alpha agonist, it administered as a racemic mixture, which means it can do a bunch of stuff

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20
Q

What is dobutamine used to treat

A
  • used to treat cardiogenic shock by providing “inotropic support”
    • when cardiac output is very low
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21
Q

Clinical uses of agonists

What receptor does phenlyephrine act on

A

alpha 1

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22
Q

What does Phenylephrine cause

A

causes vasoconstriction

22
Q

Why do we use phenylephrine

A

used to treat nasal congestion

sudafed

23
Q

What receptor does Midodrine act on

A

alpha 1

24
Q

Is Midodrine an agonist or antagonist

A

agonist

25
Q

Why do we use Midodrine

A

used for postural hypotension in autonomic failure

26
Q

How does Midodrine work for people

like what does it do for their body

A
  • it causes alpha 1 mediated vasoconstriction, which keeps up total peripheral resistance
  • therefore more blood is shunted centrally, so more able to cope with postural changes

Vasoconstriction with venoconstriction (increased capacitance)

27
Q

What medication to we also use to treat postural hypotension with

A

a mineralocorticoid to increase circulating volume (fludrocortisone)

28
Q

What is droxidopa

A

Prodrug for noradrenaline (by analogy with dopa for dopamine)

29
Q

What is the use of droxidopa

A

used for short-term in postural hypotension in autonomic failure

30
Q

Can you name two alpha 2 adrenoreceptor agonists and their uses

A

Clonidine
- centrally acting antihypertensive acts by decreasing drive
Brimonidine (direct transcutaneous vasoconstriction) for Rosacea
- to oppose this we use alpha 2 agonsit topically, causes contraction of blood vessels after being absoped by skin

31
Q

Is Doxazosin an agonist or antagonist

A

anatgonist

32
Q

Why do we use doxazosin

A

Used to treat: hypertension, Raynaud’s syndrome (inappropriate or excessive cutaneous vasoconstriction)

33
Q

What is the mechanism behind Doxazosin

what does it aim to do and how

A

Causes vasodilation, by opposing resting tone

How?
blocks alpha 1 adrenoceptors, causes vasodilation to oppose sympathetic activity

34
Q

Are beta blockers agonists or antagonists

A

antagonists

35
Q

Name some beta blockers, and what recpetors they target

A

Propranolol (beta1/beta 2), metoprolol, (beta 1)
atenolol (beta 1)

36
Q

What are the effects of beta blockers

A
  • Negative chronotropic actions
    • slows down heart rate
  • Negative inotropic actions
    • decrease contractility
  • Inhibits automaticity
    • Hence, decrease the work done by the heart
    • Anti-platelet aggregation
    • Used to treat: angina, heart failure, cardiac arrhythmias (antidysrhythmic drugs), hypertension

In agina the main use → through decreasing workload of heart

37
Q

What drug targets both alpha and beta adrenoceptors

A

Carvedilol

38
Q

What do we use carvedliol

A

heart failure

39
Q

How does carvedilol work

A

inhibits a particular cardiac potassium channel

  • block alpha-adrenoceptor
  • causes drop in blood pressure
  • which decreases total peripheral resistance
  • which decreases after load
40
Q

How do beta blockers decrease BP

A
  • Decrease cardiac output, especially during exercise, stress etc
    • may lead to “resetting” of baroreceptors (in hypertension).
  • beta 1-receptors in the kidney lead to renin release
    • renin leads to the production of angiotensins ( vasoconstriction and fluid retention).
  • Inhibit the trophic effects of catecholamines in the heart (inhibit cardiac hypertrophy associated with both hypertension and heart failure)
41
Q

What are the parasympathetic effects on the cardiovascular system

A

Heart
- Negative chronotropic action through action at the sinoatrial node
- Slow AV node conduction
- Little effect on myocardial contractility
- may be involved in vagal modulation of ventrciualr rhythm

Blood Vessels:
- Limited vasodilation, because of limited innervation (despite widespread endothelial mAChRs)
- Complicated by muscarinic receptor-induced release of NO from endothelial cells

42
Q

What is teh name of the main muscarnic recpetors on teh heart

A

mostly M2 recpetprs in the heart

mediated by mediated by Gi (inhibits adenyl cyclase)

so opposite to beta adrenergic responses

43
Q

What are the two main M2 mediated signalling pathways

A

1) Direct G-protein-meditated activation of k chnanles
-causes hyperpolarisation of cardiomyocytes

(2) Inhibition of adenylate cyclase (ADC) - opposes PKA-mediated actions on some channels

44
Q

What is the name of an antagonist that blocks M2 receptors

A

Atropine

45
Q

Does atropine only target M2 recpetors on the heart

A

NO, it can also block all M2 receptors

  • decreased secretions (mouth, airways, gut)
  • bronchodilation
  • constipation
  • urinary retention
  • pupillary dilation
  • confusion/hallucinations
46
Q

Why do we use atropine clinically

and what are the effects in these scenrioes

A

Bradycardia following MI with hypotension
-PNS slows down HR so you can increase HR by opposing PNS activation.

Excessive bradycardia with beta-blocker use
-Beta blockers reduce sympathetic drive to tone
-can block PNS actiavtion of heart

Intra-operative bradycardia
-Deep anaesthesia with supress sympathetic drive to heart
-so heart rate gets lower
-so theres atropine on standby

47
Q

Can you explain how we make noradrenaline, release and recyle it

A

Synthesis
-tyrosine is converted to DOPA (dihydroxyphenylalanine)
-DOPA is converted to dopamine
-then dopamine is converted into noradrenaline
-noradrenaline is then packaged in vesicles
-then it is exocytosed

Reuptake
-NAd is then reuprake by the noradrenaline transporter
-it is then broken down by MAO

48
Q

How do we effect the uptake of NAd and what drugs do we use

A

Uptake is mediated by NAT (noradrenaline transporter), you can block the transporter

So what drugs do this
-cocaine
-tricyclic antidepresseants (imipramine)

there’s also non neuronal uptake

49
Q

What is the main side effects of drugs that block the NAT receptor

A

cause pro-arrhythmic effects (so basically excessive arrhytmias)

Why?
-increase in spontaneous contraction can cause a pro-arrhythmic effect
-theres an accumilation od NA in extracelluar space
-you get an amplification of symapthetic drive
this increases cardiomyocytes activity (increases automaticity

50
Q

What is the other way of affecting NAD that isnt is uptake

A

You can effect MAO
-MAO breaks down Noradreanline
-if you block MAO
- you can amplify noradrengeric signalling,

51
Q

What do we use MAO inhibitors for

name some drugs

A

-have been used as anti deppresants

MAO inhibitors e.g phenelzine, iproniazid)

52
Q

What is the name of the selective MAO small b inhibtor

A

selegiline

53
Q

What is the first line treatment for hypertension in pregnancy

A

Methyldopa
- mixed mechanism of action
- DOPA (decarboxylase inhibition) so less peripheral NAd)
- so there is less synthesis of noradrenaline
- It converted dopamine beta-hydroxylase to alpha methyl norepinephrine an alpha 2 adrenoreceptor agonist
- alpha 2 agonists act in brain to drop sympathetic drive

54
Q

What drugs can affect the release NAd

A

Indirectly acting sympathomimetic amines

Drugs
-tyramine
-ephedrine
-amphetamine

55
Q

How do sympathomimetic amines work

A
  • can cause noradrenaline to be pushed out of sympathetic nerve terminals
  • by displacing nordarenline in places
  • they indirectly cause noradrenaline to activate receptors in the heart
  • have actions that mimic the sympathetic nervous system →which increases cardiac output
56
Q

What food do we find tyramine in

A

cheese

  • this can cause an increase in blood pressure
  • in conjunction with MAO inhibitors

CVS (4 decks)

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